Figure 2.

Schematic representation of promotion function of DEC1 in cell proliferation. DEC1 is inducible by HIF-1α in cancer cell. The mechanism of this interaction has
been shown to be the HIF-1α/β complex directly binding to the HIF-1 binding site in
the hypoxia response element(HRE) of the DEC1 promoter to initiate the transcription
of DEC1.The cells that lack the functional tumor suppressor von Hippel-Lindau(VHL)
express higher levels of DEC1. DEC1 is a downstream target of transforming growth
factor β signaling, which promotes the survival of cells. DEC1 transcriptionally upregulates
the expression of the survivin and signal transducer and activator of transcription
3 (STAT3). Forced expression of DEC1 selectively inhibits the activation of procaspases.